The clock genes that control circadian rhythms in mammals also contribute to other aspects of physiology, behavior, and health. One such clock gene, Bmal1, encodes a transcription factor whose inactivation in mice causes disturbances in circadian rhythms and alterations in activity level, body weight, and other physiological functions. By re-expressing the Bmal1 gene in selective tissues in Bmal1-deficient mice, McDearmon et al. show that the transcription factor exerts distinct tissue-specific functions. Circadian rhythmicity in the mutant mice was normalized only when Bmal1 was expressed in the brain, whereas normalization of the animals’ activity level and body weight required Bmal1 expression in muscle.